MEDICINAL PLANTS IN PARKINSON’S DISEASE TREATMENT: A BRIEF REVIEW OF THE RECENT DATA

MEDICINAL PLANTS IN PARKINSON’S DISEASE TREATMENT: A BRIEF REVIEW OF THE RECENT DATA

Adjia Hamadjida *, Rigobert Espoir Ayissi Mbomo, Fidèle Ntchapda and Jean Pierre Kilekoung Mingoas

Department of Neuroscience, University of Montreal, Montreal, Canada.

ABSTRACT: Parkinson's disease (PD) is a common neurodegenerative disorder that affects approximately 2% of the population aged over 65. Dopamine precursor L-3,4-dihydroxyphenylalanine (L-DOPA) is the main treatment to provide symptomatic relief for Parkinson’s disease (PD). However, with long-term administration of L-DOPA, as many as 95% of patients develop several complications. Medicinal plants (MP) and their active components have been used throughout the worldfor the management and treatment of several diseases such as PD. The World Health Organization (WHO) estimates that 80% of population in developing countries, particularly in Africa, use traditional medicine due to financial constraints. Thus, the use of medicinal plants represents the therapeutic response for populations who have difficulty accessing modern drugs and a source of income. Several MP have been administered over a long period, and they have been proven to cure PD. Therefore, this review provides a summary of recent advance of MPand their bioactive compounds involved in the treatment of PD from the year 2018up to now.

Keywords: Parkinson disease, Medicinal plants, Treatment, Bioactive compound

INTRODUCTION: Parkinson’s disease (PD) is a relentlessly neurodegenerative and progressive disease that is mainly associated with various motor and complications, including resting tremor, rigidity, bradykinesia, postural instability and gait disorder ^{1, 2}.

This neurodegenerative disorder affects approximately 1% of the population aged 60 years and over ³ and considerably undermines their quality of life. PD is pathologically characterized by slow and gradual degeneration of dopaminergic neurons in the substantia nigra compacta that leads to a decrease in the level of dopamine in the striatum, tailed nuclei and the putamen ^{4, 5}.

There is currently no available conventional treatment that either stops or reverses degenerative processes involved in the disease and the main treatment that provide symptomatic relief, improve functional capacity and quality of life in PD is the dopamine precursor L-3, 4-dihydroxyphenylalanine (L-DOPA) ⁶. However, after chronic administration, L-DOPA use is associated with the development of motor complications such as abnormal involuntary movements (AIMs), dyskinesia ⁷.

Despite being the cheapest treatment for PD, L-DOPA is not currently sustainable for thousands of PD patients around the world with a low-income because of limited availability and affordability. Thus, the discovery and development of new treatments which will not only be accessible to all, but which may also have fewer side effects represents a major challenge today. The use of plants could be an alternative for patients with PD because MP have been widely used by humans to treat several diseases throughout the world. Several studies carried out in parkinsonian rats ⁸, primates ⁹ and humans ^{10, 11} have suggested that extracts of MP and their bioactive compounds have shown to improve PD symptoms. Here, we will provide an overview of recent advances of MP and their bioactive compounds used as novel therapeutic strategies against PD.

METHODS: Many studies have been carried out in the recent years on the potential effects of numerous MP in the treatment of PD around the world. Some of them have proved to be effective and more reliable than the usual synthetic drugs. In this review, we highlighted recent studies that mainly focuse on the therapeutic effects of some MP and/or its active components on the treatment of PD symptoms. The data narrated here were assembled from recent databases PubMed, Web of Science, Science direct and Google Scholar from 2018 up to now.

Methods:

Artemisia absinthium: Artemisia absinthium (A. absinthium) popularly known as “Wormwood” is a MP that belongs to the family of Asteraceae. The plant commonly grows naturally on the rocky soils of altitude in Europe, America, Asia and some countries in Africa. In traditional medicine, A. absinthium is known for its antiseptic, antispasmodic, stomachic, cardiac stimulant, anthelmintic, and anti-inflammatory properties, and is generally used to improve memory and mental abilities ¹². In a recent study assessing the effect of Artemisia absinthium on 6-hydroxydopamine (6-OHDA)-induced toxicity in the human neuroblastoma SH-SY5Y cell line, pre-treatment of SH-SY5Y cells with ethanolic extract of A. absinthium extract (12.5 to 100 μg/mL) for 24 hours and incubated with 6-OHDA for 24 hours significantly increased the cell viability and the levels of Glutathione (GSH) and superoxide dismutase (SOD). A. absinthium also significantly decreased the level of reactive oxygen species (ROS), malondialdehyde (MDA) and cell apoptosis ¹³.

Another study reported the effects of Artemisinin, a bioactive component of Artemisia on 1-methyl-4-phenyliodine iodide (MPP⁺)-treated SH-SY5Y cells model of PD ¹⁴. In this study, Artemisinin at different concentrations significantly increased the viability of SH-SY5Y cells treated with MPP⁺ and reduced oxidative stress damage and apoptosis when compared with MPP⁺ alone. The levels of ROS and MDA were significantly reduced whereas the levels of SOD and GSH were increased.

Boswellia serrata: Boswellia is a genus in the Burseraceae family. It comprises several species traditionally used for the treatment of chronic inflammatory diseases, cerebral edema, chronic pain syndrome, gastrointestinal diseases, tumors, as well as enhancing intelligence. In a study evaluating the effects of Boswellia serrata (B. serrata) resin extract on motor dysfunction and brain oxidative stress in a 6-OHDA model of PD, treatment with B. serrata at doses of 125 and 250 mg/kg significantly decreased the net number of rotations whereas treatment at doses of 125, 250 and 500 mg/kg significantly reduced the latency and total time in comparison to 6-OHDA group ¹⁵.

Brassica juncea: The effects of Brassica juncea (B. juncea) leaf extract (200, 400, and 600 mg/kg) were evaluated on motor functions of rats with haloperidol-induced Parkinsonism. Oral administration of B. juncea improved muscles strength, motor coordination, and balance by significantly decreasing the level of catalepsy and significantly increasing the timing in hang as well as in horizontal bar test after three weeks of study as compared to haloperidol-induced Parkinsonism. In this study, B. juncea significantly increased SOD, CAT, and GSH levels and decreased MDA levels. Moreover, dopamine levels increased in rats treated with B. juncea extract at dose of 200, 400, and 600 mg/kg whereas monoamine oxidase B (MAO-B) levels significantly decreased in the brain of animals treated with B. juncea at 600 mg/kg. The extract of B. juncea at 200 mg/kg showed moderate recovery from vacuolation and dopaminergic neurons while extract-treated groups at 400 and 600 mg/kg exhibited better recovery from haloperidol-induced brain damage ¹⁶.

Carthamus tinctorius: Carthamus tinctorius (CT), also named safflower has long been used to treat cerebrovascular diseases in China. This plant contains flavonoids, which have been reported to be effective in models of neurodegenerative disease like PD. Administration of standardized CT flavonoid extract at the dose of 17.5, 35 and 70 mg/kg on rotenone-induced PD in rats significantly prevented the decrease of body weight, rotarod time and locomotion frequency and improved rearing behavior and grip strength in treated ratscompared to the rotenone group ¹⁷. Dailyoral administration of CTalso prevented thedecrease of the level of DA and its metabolites, DOPAC and HVA, as well as the levels of 5-HTand its metabolite 5-HIAA compared to the rotenone group ¹⁷.

Centella asiatica: Centella asiatica (C. asiatica) is a medicinal plant commonly used for various applications in several Asian countries ¹⁸. The effects of CA have been evaluated in rotenone-induced Parkinsonism rats model of PD ¹⁹. In this study, rats treated with CA extract have shown a significant increase in travelled distances and a higher number/intensity of dopaminergic neurons in the substantia nigra and striatum compared to PD rats. Moreover, administration of CA extract decreased MDA levels and increased SOD and catalase expression.

Thus, CA extract has been found to protect rotenone-induced Parkinsonism rats against lipid peroxidation, dopaminergic neuronal death, and locomotor deficit. The effects of CA have also been evaluated in α-synucleic transgenic models of PDusing Asiatic acid (AA), a triterpene extracted from CA ²⁰. In this study, AA significantly improved the climbing response of α-synucleic transgenic PD drosophilia with 0.5–2 mg of AA/100 g of culture medium and significantly increased cell viability in rotenone-induced SH-SY5Y cell damage. Moreover, AA also decreased the MDA levels and increased the GSH content that is induced by α-syn overexpression in PD flies. Thus, AA has shown to reduce oxidative stress against the α-syn aggregation caused by cell death, protect nerve cells, and reduced or even reverted the symptoms of PD. In another study, pretreatment with AA significantly decreased mitochondrial ROS production in a 1-methyl-4-phenyl-pyridine (MPP+)-induced neuroblastoma model of PD and protected the cells form the loss of mitochondrial membrane potential ²¹.

Ceratonia siliqua: The protective effects of aqueous extract from Ceratonia siliqua Leaves (CsAE) on 6-OHDA in Zebrafish were evaluated following immersion of CsAE (0.1, 0.3, and 1 mg/L) to zebrafish for eight consecutive days and one hour before each daily behavioral test, with 6-OHDA (250 μM). In this study, CsAE decreased the time spent and increased the total distance travelled in the novel tank diving test when compared to 6-OHDA alone. Moreover, administration of CsAE with 6-OHDA significantly improved locomotion by increasing the percentage of spontaneous alternation (in a dose-dependent manner), the number of arm entries and the total distance travelled in the Y-maze test when compared to 6-OHDA alone. CsAE (0.1, 0.3, and 1 mg/L) also shown an anti-acetylcholinesterase (AChE) effect and improved brain antioxidant status. Thus, CsAE administration (0.1, 0.3, and 1 mg/L) significantly decreased AChE and MDA level and increased SOD, CAT and GPX activity in the zebrafish brain as compared to 6-OHDA alone-treated ²².

Cinnamomum sp: Cinnamomum sp(Cinnamon) belongs to the family of Lauraceae is a widely used spice with a unique aroma and flavor ²³. The effects of Cinnamonandits main bioactive compound cinnamaldehyde has been evaluated on 6-OHDA-induced apoptosis in PC12 cells asan in vitro model of Parkinson’s disease ²⁴. In this study, cells were incubated with different concentrations of extracts, essential oils and cinnamic aldehyde (CA), the key flavor compound in Cinnamon for 24 h before exposure to 100 mm 6-OHDA.

Treatment with Cinnamon extracts and cinnamaldehyde significantly increased the viability percentage of 6-OHDA-treated cells and decreased the levels of ROS. Moreover, Cinnamon extracts and CA also protected the cells from apoptosis and significantly suppressed the activation of p44/42 pathway in PC12 cells exposed to 6-OHDA. Bae et al (2018) also used BE (2)-M17 cells to evaluate the in vitro effects of CA on MPP⁺-induced neuronal cell death. They found that when the cells were exposed to MPP⁺ for 48 h, cell viability was reduced by almost 50%.

The reduction of viability mediated by MPP⁺ was significantly recovered by CA treatment. CA also exhibited potent effects against autophagy induced by MPP⁺by decreasing the stimulation of microtubule-associated protein light chain 3 (LC3) puncta and increasing the downregulated activity of p62 in the substantia nigra. Moreover, in-vivo study evaluating the protective effects of CA in the MPTP-induced mouse model of PD ²⁵ has revealed that administration of CA significantly reduced the selective loss of TH-positive cell death (dopaminergic cell) in the substantia nigra and the severe loss of dopamine neuron fiber density in the striatum of the MPTP-administered mice. CA was also shown to enhance autophagy in a MPTP-induced mouse model of PD by inhibiting the activation of the microtubule-associated protein light chain 3 (LC3) puncta and enhancing the downregulated activity of p62 in the SN.

Ling et al reported that that gold nanoparticles (NPs) synthesized from Cinnamon protected against MPTP-induced oxidative stress, neuroinflammation, and motor deficits in MPTP-treated rat models of PD. Administration of NPs showed to improve pole-climbing capacity with a significant increased climb time as compared to MPTP induced rats that exhibited a decrease of pole-climbing. NPs also showed to decrease the muscle rigidity and the grasp strength caused by MPTP. The administration of these NPs also reduced levels of proinflammatory cytokines (TNF-a, IL-1ba, and IL-6) in the brain tissue of rats, as well as decreased ROS generation and increased SOD activity ²⁶. Administration of cinnamon metabolite increased the expression of glial cell line-derived neurotrophic factor (GDNF) in the substantia nigra pars compacta and improved locomotor activities in MPTP mouse model of PD ²⁷.

Coreopsis lanceolate: The effect of Coreopsis lanceolata flower (CLF) extracts were evaluated in MPTP/MPP+-induced mice PD model. Administration CLF extracts (50, 100 and 200 mg/kg) increased SOD, CAT activity and reduced ROS. Moreover, pretreatment with CLF (200 mg/kg) increased the Bcl-2 protein and decreased Bax compared with the MPP+ treated mice model group. In the in-vitro study, CLF also enhanced the expression of the Bcl-xL protein but reduced the expression of Bax and the cleavage of caspase-3. Thus, CLF ameliorated oxidative stress and protected neurons from MPTP/MPP+-induced apoptosis ²⁸.

Crataegus pinnatifida Bunge: The neuroprotective effect of vitexin (Vit), a flavonoid compound isolated from Crataegus pinnatifida Bunge was examined in PD models both in-vitro and in-vivo. In an in-vitro study, SH-SY5Y cellswere pretreated with various concentrations of Vit for 2 hours and incubated with 1 mM MPP+ for 24 hours. Thus, on SH-SY5Y cells, with MPP+ treatment significantly reduced cell viability, induced apoptosis, and increased Bax/Bcl-2 ratio and caspase-3 activity. However, pretreatment of Vit significantly improved these parameters induced by MPP+ treatment ²⁹.

Moreover, in-vivo study using MPTP-treated mice, pretreatment with Vit significantly reduced total locomotor activity time from the pole test and increased traction score and hanging time from traction test. The results suggested that Vit pretreatment prevented bradykinesia and alleviated the initial lesions caused by MPTP. Vit treatment also rescued the inhibited PI3K/Akt signaling pathway induced by MPTP and attenuated apoptosis by decreasing the Bax/Bcl-2 ratio and caspase-3 activity ²⁹.

Crossyne flava: In a study evaluating the effects of the total extract of Crossyne flava (CF) and its bioactive alkaloids in an in vitro MPP+ (1-methyl-4- phenylpyridinium) PD model using SH-SY5Y cells, it was observed that treatment of SH-SY5Y cells with MPP+ led to a significant reduction in SH-SY5Y cell viability when compared to the control. When SH-SY5Y cell were pre-treatment with CFprior to the addition of MPP+, cell viability was increased by 96.5%, 69.3%, and 55.3%, respectively, for the 2.5, 5, and 10 μg/mL concentrations of the extract. The isolated compounds (pancratinine B, bufanidrine, buphanisine and epibuphanisine) of CF also showed an increase of cell viability that was especially significant at the concentration of 2.5μg/mL.SH-SY5Y cells pre-treated with 2.5 μg/mL of CF and their compound before the addition of MPP+ significantly decrease the MPP+ -induced ROS generation and increase the MPP+ -induced ATP degeneration. Moreover, pre-treatment with CF and their compound prior to the addition of MPP+ led to an increase in the levels of caspase 3/7 activity in SH-SY5Y cells ³⁰.

Ginkgo biloba: In a study evaluating the effects of Ginkgo Biloba Extract (GBE) on A53T α-Synuclein Transgenic Mouse Models of PD, GBE treatment at different dose significantly improved locomotor performance (using the pole test, forced swim test, and wire-hang test) in a dose-dependent manner compared with the A53T α-Synuclein transgenic mice treated with normal saline. GBE also improved the activity of different antioxidant enzymes in α-Synuclein A53T Transgenic Mice. Thus, GBE treatment significantly increased the SOD and GSH-PX activities and reduced MDA expression in A53T α-synuclein transgenic mice in a dose-dependent manner compared with the A53T α-Synuclein transgenic mice treated with normal saline ³¹.

Ginkgolide B (GB), a diterpenoid lactone and Protocatechuic acid (PCA), the main compound of organic acids, both extracted from GBE have shown many biological activities including neuroprotective and antioxidant effects ^{32, 33}. Thus, synergistic neuroprotective effects of GB and PCA were evaluated on the treatment of PD. Combined treatment with GB and PCA on rotenone-induced PC12 cells significantly increased cell viability and improved cell morphology as compared to those of the single treatment of GB or PCA. Moreover, the combined treatment with GB and PCA in rotenone-induced PC12 cells significantly decreased the level of ROS. GSH, SOD and CAT content also significantly increased after the combination treatment of GB and PCA in rotenone-damaged cells. The addition of combined treatment with GB and PCA significantly decreased the expressions of Bax, Caspase-3 and Cytochrome C and increased Bcl-2 expression ³⁴. In the MPTP (30 mg/kg)-induce PD in C57BL/6 mice, the combination of GB and PCA treatment improved the motor ability (pole-climbing time and the suspension score) of the mice. The levels of GSH, SOD and CAT were increased in the midbrain after 21 days of the combination treatment of GB and PCA. The number of TH positive cells were also increased in the combined treatment group ³⁴.

Mucuna pruriens: Mucuna pruriens, commonly known as Mucuna or velvet bean from the Fabaceae family has been used in Indian traditional medicine for curing several brain diseases such as PD. Several studies have suggested that extracts of Mucuna pruriens (MPE) may be used to improve PD motor symptoms. The anti-PD effects of MPE were evaluated in human SH-SY5Y neuroblastoma cells, Caenorhabditis elegans, and Drosophila melanogaster models. Treatment with MPE (12.5, 25 and 50 μg/mL) increased SH-SY5Y cell viability compared with the 6-OHDA treated group by 11.9%, 38.5%, and 23.9%, respectively. MPE at dose of 20 and 40 μg/mL significantly increased the survival time of C. elegans compared with MPP+ treated group alone. In 6-OHDA and rotenone induce PD in D. melanogaster, MPE significantly increased the climbing distance as compared with flies that were treated with 6-OHDA or rotenone alone ³⁵.

Paeonia suffruticosa: Paeonia suffruticosa often referred to as Mu Dan Pi or Moutan Cortex Radicis has a long history of being used in chinese medicine for treatment of pain, spasms, and inflammation. The therapeutic effects of Paeonia suffruticosa in a 6-OHDA-induced PD model has been evaluated using the hexane, butanol, and water fractions of Paeonia suffruticosa extract (PS). In this study, treatment with the PS fractions significantly decreased the number of net turns in the behavioral rotation experiment and significantly increased the number of TH-positive cells in the substantia nigra pars compacta (SNpc) region as compared with the 6-OHDA group. The in vitro effects of PS fractions in a 6-OHDA-induced B65 neuronal cell were also evaluated. Treatment with hexane or distilled water fractions of PS reduced apoptotic cell death induced by 6-OHDA neurotoxicity and inhibited nitric oxide production and neuronal nitric oxide synthase expression ³⁶.

Punica granatum: Punica granatum from the Punicaceae family is widely used to have medicinal properties. PG contains variable phytochemicals that were referenced to exert antioxidant and anti-inflammatory impacts ³⁷. Oral administration of 500 mg/kg of Punica granatum seed extract (PG) or 5 ml of 1:40 dilution of PG juice led to a significant increase of TH protein expression, DA levels, and its metabolite DOPAC in the paraquat (PQ)-induced mouse model of Parkinson’s disease. Oral administration of either PG seed or juice significantly increased the ATP levels when compared to PQ (alone)-induced mice. Treatment of PQ-induced mice with oral administration of PG (seed of juice) led to a significant decrease in MDA levels and a substantial increase in the striatal activities of SOD, GPx, and CAT when compared with the PQ (alone)-treated group. Treatment of PQ-induced mice with PG (seed of juice) significantly decreased the striatal levels of TNF-α, IL-1β, CD11b, TGF-β and significantly increased the levels of IL-10,GDNFwhen compared with PQ (alone)-treated mice ³⁸.

Vitex negundo: Vitex negundo Linn, commonly known as the Chinese chaste tree, five-leaved chaste tree, or horseshoe vitex, or nisinda is a member of the Verbenaceae family with a large aromatic shrub with quadrangular, densely whitish, tomentose branch lets. It is widely used in folk medicine, particularly in South and Southeast Asia. In the study evaluating the effect of Vitex negundo leaf extract (VNL) in Haloperidol induced PD in rats, long term treatment with VNL extract at dose of 100, 200 and 400 mg/kg increased the performance time(grip strength) and locomotion whereas the escape latency time (ELT)decreased compared to the negative control group.

Treatment with VNL extract remarkably decreased the level of AChE, BChE in both cortex and hippocampus compared to the negative control group which received only haloperidol. Treatment with VNL extract also significantly decreased the level of MDA and increased the levels of GSH, SOD and Dopamine on whole brain compared to the negative control ³⁹.

Withania somnifera (L.): Withania somnifera is native to India, China, Nepal, and Yemen and belongs to the Solanaceae family. It has been traditionally used as an anti- inflammatory and anti-cancer agent, nerve-tonic, and proven to have therapeutic properties in many neurological and cognitive disorder ⁴⁰. In a study evaluating the neuroprotective effects of Withania somnifera root extract powder (KSM-66) on 6-OHDA-induced neurotoxicity in SH-SY5Y cells, administration of KSM-66 (0.25 to 1 mg/ml) before and after treatment of SH-SY5Y cells with 6-OHDA significantly increased viability of SH-SY5Y cells. Interestingly, KSM-66 significantly increased glutathione peroxidase activity and thioltransferase activity upon preor post6-OHDA treatment. KSM-66 also modulated oxidative response proteins by increasing peroxiredoxin-I and VGF expression and decreasing vimentin proteins upon 6-OHDA pre or post treatments. In addition, Pre-treatment of SH-SY5Y cells with KSM-66 decreased protein-glutathionylation levels in the cells treated with 6-OHDA ⁴¹.

CONCLUSION: Medicinal plants and their active compounds have shown a beneficial potential to treat various diseases such as PD symptoms. In this review, we provide an overview of several medicinal plants and their active compounds as potential therapies for the treatment of PD. The neuroprotective effect of these MP and their compounds are mainly mediated via reduction of oxidative stress and neuro-inflammation resulting in the induction of PD.

ACKNOWLEDGEMENTS: Nil

CONFLICTS OF INTEREST: Nil

REFERENCES:

1. Fahn S: Classification of movement disorders. Mov Disord 2011; 26: 947-957. 2011/06/01. DOI: 10.1002/mds.23759.
2. Bloem BR, Okun MS and Klein C: Parkinson's disease. Lancet 2021; 397: 2284-2303. 20210410. DOI: 10.1016/s0140-6736(21)00218-x.
3. Kwan C, Frouni I and Bedard D: Ondansetron, a highly selective 5-HT3 receptor antagonist, reduces L-DOPA-induced dyskinesia in the 6-OHDA-lesioned rat model of Parkinson's disease. Eur J Pharmacol 2020; 871: 172914. 2020/01/12. DOI: 10.1016/j.ejphar.2020.172914.
4. Li H, Yu Z and Zhang W: Misfolded protein aggregation and altered cellular pathways in neurodegenerative diseases. STE Medicine 2020; 1: 63. DOI: 10.37175/stemedicine.v1i4.63.
5. Johnson ME, Stecher B and Labrie V: Triggers, facilitators, and aggravators: redefining parkinson’s disease pathogenesis. Trends in Neurosciences 2019; 42: 4-13. DOI: 10.1016/j.tins.2018.09.007.
6. Tarakad A and Jankovic J: Diagnosis and management of parkinson's disease. Semin Neurol 2017; 37: 118-126. 2017/05/17. DOI: 10.1055/s-0037-1601888.
7. Hely MA, Morris JG and Reid WG: Sydney Multicenter Study of Parkinson's disease: non-L-dopa-responsive problems dominate at 15 years. Mov Disord 2005; 20: 190-199. 2004/11/20. DOI: 10.1002/mds.20324.
8. Liang W, Yao L and Chen J: Therapeutic and Neuroprotective Effects of Bushen Jianpi Decoction on a Rotenone-Induced Rat Model of Parkinson’s Disease. Evidence-Based Complementary and Alternative Medicine 2022; 2022: 1-15. DOI: 10.1155/2022/9191284.
9. Lieu CA, Venkiteswaran K and Gilmour TP: The Antiparkinsonian and Antidyskinetic Mechanisms of Mucuna pruriens in the MPTP-Treated Nonhuman Primate. Evid Based Complement Alternat Med 2012; 2012: 840247. 2012/09/22. DOI: 10.1155/2012/840247.
10. Singhal B, Lalkaka J and Sankhla C: Epidemiology and treatment of Parkinson's disease in India. Parkinsonism & Related Disorders 2003; 9: 105-109. DOI: 10.1016/s1353-8020(03)00024-5.
11. Katzenschlager R, Evans A and Manson A: Mucuna pruriens in Parkinson's disease: a double blind clinical and pharmacological study. J Neurol Neurosurg Psychiatry 2004; 75: 1672-1677. 2004/11/19. DOI: 10.1136/jnnp.2003.028761.
12. Wake G, Court J and Pickering A: CNS acetylcholine receptor activity in European medicinal plants traditionally used to improve failing memory. Journal of Ethnopharmacology 2000; 69: 105-114. DOI: 10.1016/s0378-8741(99)00113-0.
13. Rashidi R, Ghorbani A and Rakhshandeh H: Protective effect of Artemisia absinthium on 6-hydroxydopamine-induced toxicity in SH-SY5Y cell line. Avicenna Journal of Phytomedecine 2021; 11: 238-246.
14. Yan J, Ma H and Lai X: Artemisinin attenuated oxidative stress and apoptosis by inhibiting autophagy in MPP+-treated SH-SY5Y cells. Journal of Biological Research-Thessaloniki 2021; 28. DOI: 10.1186/s40709-021-00137-6.
15. Parvaneh Doaee, Ziba Rajaei and Mehrdad Roghani: Effects of Boswellia serrata resin extract on motor dysfunction and brain oxidative stress in an experimental model of Parkinson’s disease. Avicenna Journal of Phytomedecine 2019; 281-290.
16. Saleem U and Bibi S Shah. MA: Anti-Parkinson’s evaluation of Brassica juncea leaf extract and underlying mechanism of its phytochemicals. Frontiers in Bioscience-Landmark 2021; 26: 1031. DOI: 10.52586/5007.
17. Ablat N, Liu R and Ablimit M: Preventive effects of a standardized flavonoid extract of safflower in rotenone-induced Parkinson's disease rat model. Neuropharmacology 2022; 217: 109209. 20220805. DOI: 10.1016/j.neuropharm.2022.109209.
18. Wong JH, Barron AM and Abdullah JM: Mitoprotective Effects of Centella asiatica (L.) Urb.: Anti-Inflammatory and Neuroprotective Opportunities in Neurodegenerative Disease. Frontiers in Pharmacology 2021; 12: 687935. 2021/07/17. DOI: 10.3389/fphar.2021.687935.
19. Teerapattarakan N, Benya-Aphikul H and Tansawat R: Neuroprotective effect of a standardized extract of Centella asiatica ECa233 in rotenone-induced parkinsonism rats. Phytomedicine 2018; 44: 65-73. DOI: 10.1016/j.phymed.2018.04.028.
20. Ding H, Xiong Y and Sun J: Asiatic Acid Prevents Oxidative Stress and Apoptosis by Inhibiting the Translocation of alpha-Synuclein Into Mitochondria. Front Neurosci 2018; 12: 431. 20180628. DOI: 10.3389/fnins.2018.00431.
21. Chen D, Zhang XY and Sun J: Asiatic Acid Protects Dopaminergic Neurons from Neuroinflammation by Suppressing Mitochondrial ROS Production. Biomolecules & Therapeutics 2019; 27: 442-449. DOI: 10.4062/biomolther.2018.188.
22. Abidar S, Boiangiu RS and Dumitru G: The Aqueous Extract from Ceratonia siliqua Leaves Protects Against 6-hydroxydopamine in Zebrafish: Understanding the Underlying Mechanism. Antioxidants (Basel) 2020; 9 2020/04/12. DOI: 10.3390/antiox9040304.
23. Maiolo SA, Fan P and Bobrovskaya L: Bioactive constituents from cinnamon, hemp seed and polygonum cuspidatum protect against H 2 O 2 but not rotenone toxicity in a cellular model of Parkinson's disease. Journal of Traditional and Complementary Medicine 2018; 8: 420-427. DOI: 10.1016/j.jtcme.2017.11.001.
24. Ramazani E, Yazdfazeli M and Emami SA: Protective effects of Cinnamomum verum, Cinnamomum cassia and cinnamaldehyde against 6-OHDA-induced apoptosis in PC12 cells. Molecular Biology Reports 2020; 47: 2437-2445. DOI: 10.1007/s11033-020-05284-y.
25. Bae WY, Choi JS and Jeong JW: The Neuroprotective Effects of Cinnamic Aldehyde in an MPTP Mouse Model of Parkinson’s Disease. International Journal of Molecular Sciences 2018; 19: 551. DOI: 10.3390/ijms19020551.
26. Ling L, Jiang Y and Liu Y: Role of gold nanoparticle from Cinnamomum verum against 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) induced mice model. J Photochem Photobiol B 2019; 201: 111657. 20191028. DOI: 10.1016/j.jphotobiol.2019.111657.
27. Patel D, Jana A and Roy A: Cinnamon and its Metabolite Protect the Nigrostriatum in a Mouse Model of Parkinson's Disease Via Astrocytic GDNF. J Neuroimmune Pharmacol 2019; 14: 503-518. 20190522. DOI: 10.1007/s11481-019-09855-0.
28. Kim HD, Lee JY and Park JY: Neuroprotective Effects of Coreopsis lanceolata Flower Extract against Oxidative Stress-Induced Apoptosis in Neuronal Cells and Mice. Antioxidants (Basel) 2021; 10 2021/07/03. DOI: 10.3390/antiox10060951.
29. Hu M, Li F and Wang W: Vitexin protects dopaminergic neurons in MPTP-induced Parkinson’s disease through PI3K/Akt signaling pathway. Drug Design, Development and Therapy 2018; Volume 12: 565-573. DOI: 10.2147/dddt.s156920.
30. Omoruyi SI, Ibrakaw AS and Ekpo OE: Neuroprotective Activities of Crossyne flava Bulbs and Amaryllidaceae Alkaloids: Implications for Parkinson's disease. Molecules 2021; 26 2021/07/03. DOI: 10.3390/molecules26133990.
31. Kuang S, Yang L and Rao Z: Effects of Ginkgo Biloba Extract on A53T α-Synuclein Transgenic Mouse Models of Parkinson’s Disease. Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 2018; 45: 182-187. DOI: 10.1017/cjn.2017.268.
32. Maclennan KM, Darlington CL and Smith PF: The CNS effects of Ginkgo biloba extracts and ginkgolide B. Progress in Neurobiology 2002; 67: 235-257.
33. Scholtyssek H, Damerau W and Wessel R: Antioxidative activity of ginkgolides against superoxide in an aprotic environment Chemico-Biological Interactions 1997; 106: 183-190.
34. Wu T, Fang X and Xu J: Synergistic Effects of Ginkgolide B and Protocatechuic Acid on the Treatment of Parkinson’s Disease. Molecules 2020; 25: 3976. DOI: 10.3390/molecules25173976.
35. Johnson S, Park H and Dasilva N: Levodopa-Reduced Mucuna pruriens Seed Extract Shows Neuroprotective Effects against Parkinson’s disease in Murine Microglia and Human Neuroblastoma Cells, Caenorhabditis elegans, and Drosophila melanogaster. Nutrients 2018; 10: 1139. DOI: 10.3390/nu10091139.
36. Choi YG, Hong YM and Kim LH: Moutan Cortex Radicis inhibits the nigrostriatal damage in a 6-OHDA-induced Parkinson's disease model. Chinese Journal of Natural Medicines 2018; 16: 490-498. DOI: 10.1016/s1875-5364(18)30084-0.
37. Lansky EP and Newman RA: Punica granatum (pomegranate) and its potential for prevention and treatment of inflammation and cancer. Journal of Ethnopharmacology 2007; 109: 177-206. DOI: 10.1016/j.jep.2006.09.006.
38. Fathy SM, El-Dash HA and Said NI: Neuroprotective effects of pomegranate (Punica granatum L.) juice and seed extract in paraquat-induced mouse model of Parkinson's disease. BMC Complement Med Ther 2021; 21: 130. 2021/04/28. DOI: 10.1186/s12906-021-03298-y.
39. Vannur A, Biradar PR and Patil V: Experimental validation of Vitex negundo leaves hydroalcoholic extract for neuroprotection in haloperidol induced parkinson’s disease in rat. Metabolic Brain Disease 2022. DOI: 10.1007/s11011-021-00878-2.
40. Roy A and Datta S. Medicinal plants against ischemic stroke. Curr Pharm Biotechnol 2020 2020/12/12. DOI: 10.2174/1389201021999201209222132.
41. Wongtrakul J, Thongtan T and Kumrapich B: Neuroprotective effects of Withania somnifera in the SH-SY5Y Parkinson cell model. Heliyon 2021; 7: 08172.
    

    ---

    How to cite this article:

    Hamadjida A, Mbomo REA, Ntchapda F and Mingoas JPK: Medicinal plants in Oarkinson’s disease treatment. a brief review of the recent data. Int J Pharm Sci & Res 2023; 14(10): 4756-63. doi: 10.13040/IJPSR.0975-8232.14(10). 4756-63.

    ---

    All © 2023 are reserved by International Journal of Pharmaceutical Sciences and Research. This Journal licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License.